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Biomedical subjects

L N Maslov

Publications and source records attributed to L N Maslov.

At least 145 records · Page 8Linked to original sources
PubMedDate not supplied

[Using cytokines to stimulate neoangiogenesis and cardiac regeneration].

Data published on the use of cytokines for the stimulation of neoangiogenesis and cardiac regeneration have been systematized. There is evidence that insulin-like growth factor (IGF1) can stimulate proliferation of cardiomyocytes; hepatocyte growth factor (HGF) does not influence the mitosis of cardiac cells, but prevents post-infarction remodeling of heart; vascular endothelial growth factor (VEGF) stimulates proliferation of endothelial cells in vitro and neovasculogenesis in the ischemic heart in vivo for both animals and humans; fibroblast growth factor (FGF) can also induce neovasculogenesis in the ischemic heart; granulocyte-colony-stimulating factor (G-CSF) can mobilize stem cells and endothelial progenitor cells in bone marrow, which are involved in neoangiogenesis and cardiac regeneration; erythropoietin can mobilize endothelial progenitor cells from bone marrow and induce neovascularization of ischemic tissue in vivo. It is suggested that VEGF, G-CSF and erythropoietin are the most promising compounds for the stimulation of neoangiogenesis and cardiac regeneration in patients with myocardial infarction.

Animals↗
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[Opioid peptides in the dynamics of "physiological" and "pathological" stress].

Clinical studies showed that short-term "physiological" stress (bicycle ergometry) did not cause increase of the blood plasma enkephalin content. Moderate-term (60-minute) stress, according to O. Desiderato, causes a rise of the blood enkephalin level in rats. It is supposed that such a reaction of the opioid system is characteristic of borderline conditions between normal and pathological states in stress. Severe "pathological" stress (myocardial infarction, experimental coronary occlusion, 6-hour stress after O. Desiderato) in rats led to a decrease of the concentration of enkephalins in the blood and disorders of their secretion and storage in the adrenals. It is suggested that changes of the activity of the opioid system are a predictor of the transition of a "physiological" stress to a "pathological" stress.

Adrenal Glands↗
PubMedDate not supplied

[Adrenergic regulation of the level of enkephalins in the myocardium].

Content of enkephalins was increased in myocardium after administration of tyramine (liberator of endogenous catecholamines). Neoepinephrine decreased content of Met-enkephalin in heart. Catecholamines circulating in blood exhibited less distinct effect on content of opioid peptides in myocardium as compared with endogenous free catecholamines. Inverse correlation was found between content of cAMP and Met-enkephalin in myocardium. All the pharmacological drugs studied could exhibit the mediatory effects on opioid peptides in heart via alterations in activity of vegetative nervous system affecting the myocardium.

Animals↗
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[Changes in brain energy metabolism in experimental cerebral hemorrhage].

Intracerebral hemorrhage impaired the functional activity of rat brain mitochondria. After experimental insult the rate of succinate and alpha-ketoglutarate oxidation was decreased at the states 3 and 4 in brain mitochondria as well as in presence of 2,4-dinitrophenol. The rate of phosphorylation was also decreased in oxidation of both NAD- and FAD-dependent substrates.

Animals↗
PubMedDate not supplied

[Effect of gamma-oxybutyrate on energy metabolism and the cyclic nucleotide level in nerve tissue in experimental intracerebral hemorrhage].

Experimental intracerebral hemorrhage (EICH) was shown to cause a disorder of the functional state of the brain mitochondria. The rate of oxidation of NAD- and FAD-linked substrates in 3 and 4 states decreased 1 and 24 hours after hemorrhage. An injection of gamma-hydroxybutyrate 1 hour before decapitation increased the rate of mitochondrial respiration. EICH was found to increase cGMP level and to decrease cAMP level. A combined action of hemorrhage and gamma-hydroxybutyrate produced a greater lowering of cAMP level and an elevation of cGMP level.

Animals↗
PubMedDate not supplied

[An experimental study of the pharmacological activity of opiate receptor ligands on models of adrenaline-induced arrhythmias].

The influence of intracerebroventricular injection of opioid peptides on the incidence and severity of ventricular arrhythmia induced by intravenous administration of epinephrine was studied. It was found that DAGO, a selective mu-agonist, and DADLE, a nonselective delta-agonist, reduce the incidence and severity of cardiac arrhythmia in rats. On the contrary, DSLET, a selective delta-agonist, and Dynorphin A 1-13 (kappa-agonist), potentiates epinephrine-induced arrhythmias. beta-Endorphin do not affect the arrhythmia. The activation of cerebral mu-opioid receptors is shown to prevent the appearance of arrhythmia. On the contrary, the activation of delta- and kappa-receptors induces the appearance of arrhythmia.

Animals↗
PubMedDate not supplied

[The cardioprotective and antiadrenergic activity of an extract of Rhodiola rosea in stress].

The course of administration of Rhodiola rosea extract was studied for effects on the pattern of stress-induced cardiac damage which was assessed by 99mTc-pyrophosphate accumulation in the heart. Rhodiola rosea was found to prevent stress-induced cardiac damage. Simultaneously, myocardial catecholamines and cAMP levels were measured. Rhodiola rosea was ascertained to prevent both stress-induced catecholamine release and higher cAMP levels in the myocardium. Moreover, the adaptogen prevented lower adrenal catecholamines during stress. The findings suggest that the antistressor and cardioprotective effects of Rhodiola rosea are associated with limited adrenergic effect on the heart.

Adrenergic Antagonists↗
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[The limitation of the intensity of the stress reaction under open-field test conditions through the adaptation of rats to cold and physical loading].

Male Wistar rats' adaptation to the periodical cold exposure (3 hours daily, 6 times a week within 2 months at the air temperature of 1-2 degrees C) and to the exercise training (swimming 1 hour daily, 6 times a week within 2 months at the water temperature of 32-33 degrees C) was resulted in a limitation of motional and vegetative manifestations of the stress reaction in the "open field" test. Activation of the stress limiting systems in the organism could be one of the main causes of these adaptive effects. There was an elevation of beta-endorphin concentration and that of the ratio "prostacycline/thromboxane" in some tissues of adapted animals.

Adaptation, Physiological↗
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[The role of endogenous opioid peptides in the mechanisms of the antiarrhythmic effect of adaptation].

A decrease in severity and incidence rate of the epinephrine- or CaCl2-induced arrhythmias was found in the rats adapted to stress. An increase of the beta-endorphin and enkephalin levels was revealed in the brain areas, heart, suprarenal glands and in the blood plasma of such rats. Naloxone eliminated the antiarrhythmic effect of the adaptation, as well as D-kyotorphin. The antiarrhythmic effect seems to result from an increase of the endogenous opioid peptides level.

Adaptation, Physiological↗
PubMedDate not supplied

[Pathogenesis of impaired cardiac electric stability in experimental hypodynamia].

The decreased ventricular fibrillation threshold (VFT) in the first 5 days of restriction results from stress-induced changes in myocardial autonomic innervation, as shown by elevated cardiac content of cAMP and lowered levels of cGMP, and a rise in the plasma concentrations of corticosterone and deoxycorticosterone. Ultimately, these changes enhance cardiomyocyte membranous permeability of calcium ions and, hence, lower VFT. Impaired cardiac electric stability in the late inactivity period (50 days) is also associated with the enhanced permeability of cardiomyocyte membranes; however, the nature of this phenomenon remains unclear and calls for further studies.

Animals↗
PubMedDate not supplied

[The role of the opioid system in body adaptation and protection of the heart in stress].

Literary data and the results of our own studies on the role of opioid neuropeptides in the adaptation of organism and heart protection under the action of extreme factors were analysed. The data on the cardioprotective, antiarrhythmic, neurohumoral, antistressor effects of enkephalins are grown. Possible mechanisms and the role of various populations of opiate receptors in the realisation of opioid peptides' adaptation effects are studied. The key role of endogenous opiate system in the mechanism of cardioprotective effects of natural adaptogens and adaptation is established.

Adaptation, Physiological↗
PubMedDate not supplied

[Effect of cold stress on the contractile activity, carbohydrate and energy metabolism in the isolated rat heart].

Acute cold stress (-20 degrees C for 4 hours) in rats causes profound contractile changes in the heart isolated and perfused by the Langendorf method. This reduced contraction amplitudes and increased heart rates. The decreased contraction amplitudes was associated with inadequate ATP formation. While changing perfusion of post-stress isolated heart, myocardial rigidity slowed down, which seemed to be associated with activated glycolysis. There were no signs of cardiomyocytic lesion after cold stress. Reduced coronary flow is the only abnormal effect of acute cold stress under these conditions. High cardiac resistance to the damaging effect of cold is likely to be related to increased processes of glycolysis and glycogenolysis in the cardiomyocytes.

Animals↗
PubMedDate not supplied

[The effect of lithium chloride on the desynchronization of "reserpine-induced depression"].

Lithium chloride (5 mg/kg i.m. for 10 days in the morning but not in the evening) prevented effectively desynchronization of "reserpine depression" in mice and rats: the spectra and structure of the rhythms of behavioral parameters (open field), body temperature, content of serotonin and its metabolites in the brain and that of glucocorticoids in blood plasma were almost the same as those in intact animals; the circadian harmony of all parameters were correlated in the best manner and their mean circadian values were restored.

Adrenergic Uptake Inhibitors↗
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[The mechanism of the anti-arrhythmia action of mu-opioid-receptor agonists in a model of CaCl2-induced arrhythmias: the role of the autonomic nervous system].

It was established that selective ligands of the mu-opioid receptors DAGO and DALDA exhibit antiarrhythmic activity on a model of CACl2-induced arrhythmias when infused intravenously in a dose of 0.2 mg/kg. The autonomic nervous system does not take part in realization of the antiarrhythmic effect of DAGO and DALDA. It is supposed that this effect of DAGO and DALDA is associated with activation of cardiac mu-opioid receptors.

Animals↗
PubMedDate not supplied

[The participation of the mu-, delta- and kappa-opioid receptors in the realization of the anti-arrhythmia effect of Rhodiola rosea].

A course of the adaptogen extractum Rhodiola rosea (3.5 ml/kg given per os daily for 8 days). produces am antiarrhythmic effect on models of epinephrine-induced arrhythmia. Blockade of mu-opiate receptors (OR) by naloxone (0.2 mg/kg) and delta-OR by ICI 174.864 (2.5 mg/kg) had no effect on the resistance of the heart of rats adapted to epinephrine. Higher doses of naloxone reduced significantly the antiarrhythmic effect of extr. Rhodiola. The antiarrhythmic effect of the extract is assumed to be related to activation of the opioid system and stimulation of kappa-OR.

Adaptation, Physiological↗
PubMedDate not supplied

[The participation of the central and peripheral kappa-opiate receptors in the mechanism of the anti-arrhythmia action of benzeneacetamide derivatives].

When injected intraperitoneally in a dose of 8 mg/kg, U-62066, the selective agonist of kappa-opioid receptors, exhibits antiarrhythmic properties in epinephrine-induced arrhythmias in rats. In cerebroventricular injection, the kappa-agonists U-50,488 and [D-ala2]-dynorphin A(1-13) manifest proarrhythmic properties. Preliminary administration of the kappa-antagonist nor-binaltorphimine completely removes the proarrhythmic and antiarrhythmic effect of kappa-agonists. The antiarrhythmic effect of U-62006 is believed to be associated with activation of peripheral kappa-receptors.

Acetamides↗